title: RNAi-mediated knockdown of cyclooxygenase2 inhibits the growth, invasion and migration of SaOS2 human osteosarcoma cells: a case control study.
abstract: BACKGROUND
  Cyclooxygenase2 (COX-2), one isoform of cyclooxygenase proinflammatory enzymes, is responsible for tumor development, invasion and metastasis. Due to its role and frequent overexpression in a variety of human malignancies, including osteosarcoma, COX-2 has received considerable attention. However, the function of COX-2 in the pathogenesis of cancer is not well understood. We examined the role of COX-2 in osteosarcoma.
  
  
  METHODS
  We employed lentivirus mediated-RNA interference technology to knockdown endogenous gene COX-2 expression in human osteosarcoma cells (SaOS2) and analyzed the phenotypical changes. The effect of COX-2 treatment on the proliferation, cell cycle, invasion and migration of the SaOS2 cells were assessed using the MTT, flow cytometry, invasion and migration assays, respectively. COX-2, vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) mRNA and protein expression were detected by RT-PCR and western blotting.
  
  
  RESULTS
  Our results indicate that a decrease of COX-2 expression in human osteosarcoma cells significantly inhibited the growth, decreased the invasion and migration ability of SaOS2 cells. In addition, it also reduced VEGF, EGF and bFGF mRNA and protein expression.
  
  
  CONCLUSIONS
  The COX-2 signaling pathway may provide a novel therapeutic target for the treatment of human osteosarcoma.
authors.affiliation: Department of Orthopaedics, Affiliated First People's Hospital, Shanghai Jiao Tong University, 100 Haining Road, Shanghai 200080, China.
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Zhao
authors.forename: Chuan
authors.initials: C
authors.lastname: Wang
authors.forename: Jiaxue
authors.initials: J
authors.lastname: Zhu
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Shuanghai
authors.initials: S
authors.lastname: Dong
authors.forename: Guoqiao
authors.initials: G
authors.lastname: Zhang
authors.forename: Jiwei
authors.initials: J
authors.lastname: Tian
mesh_terms: D001859:Bone Neoplasms / Q000201:enzymology / Q000473:pathology*; D016022:Case-Control Studies; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D051546:Cyclooxygenase 2 / Q000235:genetics*; D005434:Flow Cytometry; D005562:Formazans; D055785:Gene Knockdown Techniques; D006801:Humans; D009361:Neoplasm Invasiveness; D012516:Osteosarcoma / Q000201:enzymology / Q000473:pathology* / Q000628:therapy*; D034622:RNA Interference; D013778:Tetrazolium Salts
chemical_list: D005562:Formazans; D013778:Tetrazolium Salts; C079782:MTT formazan; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human